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Exam 2 Flashcards

1
Q

4 types of drugs that affect the respiratory system

A
  1. Bronchodilators
  2. Anti-inflammatory agents
  3. Antihistamines
  4. Medications for Colds, Coughs, Nasal Decongestion
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2
Q

3 types of bronchodilators

A
  1. Adrenergics
  2. Anticholinergics
  3. Xanthine or “oophyllines”
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3
Q

3 types of anti-inflammatory medications

A
  1. Corticosteroids
  2. Mast Cell Stabilizers
  3. Leukotriene Inhibitors
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4
Q

inhalant abuse can cause what kind of injury?

A

Permanent injury to the brain, liver, kidneys, heart, and lungs

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5
Q

Expectorants (function, example)

A

liquefy secretions

ex. Guaifenesin

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6
Q

Mucolytic (function, example)

A

liquefies mucus

ex. Normal saline, Acetylcysteine

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7
Q

Cold remedies (function, example)

A

combination of antihistamine, nasal decongestant and a mild analgesic

ex. Nyquil

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8
Q

Antitussives (function, 2 types)

A

Suppress a cough

  1. Central acting
  2. Peripherally acting
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9
Q

Central acting Antitussives (2 types, examples of each)

A

Opioid: codeine
- Examples: Hycotuss, Hycodan

Non-opioid: dextromethorphan
- Example: Robitussin DM

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10
Q

Peripherally acting Antitussive: example

A

glycerin

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11
Q

3 nasal decongestant contraindications

A
  1. HTN
  2. CAD (coronary artery disease)
  3. Arrhythmias
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12
Q

how do nasal decongestants work, and what are some examples?

A

they relieve nasal obstruction and discharge through vasoconstriction

this reduces fluid loss from blood vessels which decreases inflammation and mucus production

ex. Phenylephrine (Neosynephrine), Pseudoephedrine (Sudafed)

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13
Q

5 drugs to treat colds and coughs

A
  1. Nasal decongestants
  2. Antitussives
  3. Expectorants
  4. Mucolytics
  5. Cold remedies
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14
Q

1st Generation Antihistamine is ____, and the prototype is:

A

Non-selective

Diphenhydramine (Benadryl)

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15
Q

2nd Generation Antihistamine is more selective for ____ than ____. Some examples are:

A

More selective for peripheral H1 receptors than CNS

So, fewer ADEs

Examples:
Zyrtec
Allegra
Claritan

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16
Q

5 situations when it is appropriate to use Diphenhydramine (Benadryl)

A
  1. Allergic rhinitis
  2. Mild Anaphylaxis
  3. Drug allergies
  4. Blood transfusion reaction
  5. Contact dermatitis
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17
Q

common ADE of Benadryl

A

drowsiness, sedation, dizziness, Thickening of bronchial secretions

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18
Q

serious ADE of Benadryl

A

Hemolytic anemia

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19
Q

Benadryl contraindications

A

Allergy to med

Use of other CNS meds:
ETOH (ethanol), Antianxiety, sedative-hypnotics, opioids

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20
Q

5 situations when you should use Benadryl cautiously

A
  1. UA retention
  2. BPH
  3. tachycardia
  4. arrhythmias
  5. narrow angle glaucoma
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21
Q

Type I allergic reaction

A

Immediate hypersensitivity

ex: rhinitis to anaphylactic shock

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22
Q

Type II allergic reaction

A

damage to cell surface

Ex: blood transfusion reaction

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23
Q

Type III allergic reaction

A

antigen-antibody formation

ex. Some types of arthritis, Lupus

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24
Q

Type IV allergic reaction

A

delayed hypersensitivity

Ex: poison ivy, transplant rejection

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25
Q

Anticholinergic effects of antihistamines

A

Dry mouth, nose, throat
Blurred Vision
UA Retention
Anorexia, N/V, Constipation

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26
Q

paradoxical reaction to antihistamines

A

e.g. when kid goes crazy on benadryl

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27
Q

how do antihistamines work?

A

they bind to central and peripheral H1 receptors

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28
Q

what 5 effects can histamine release cause?

A
  1. Bronchoconstriction
  2. Cough
  3. Increased capillary permeability
  4. Increased mucus production
  5. Stimulation of sensory peripheral nerve endings
  6. Dilation of capillaries
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29
Q

Anticholinergic bronchodilators: prototype

A 
Atropine
ipratropium bromide (Atrovent)
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30
Q

Anticholinergic bronchodilators: uses

A

Not for acute treatment
Used for daily maintenance
Tiotropium (Spiriva)

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31
Q

serious ADE of anticholinergic bronchodilators

A

bronchospasm, arrhythmias

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32
Q

common ADE of anticholinergic bronchodilators

A

cough and anticholinergic effects

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33
Q

Absolute contraindication for anticholinergic bronchodilators

A

allergy to med, soybeans, peanuts

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34
Q

what are the early signs of hypoxia?

A

confusion, restlessness, increased HR and RR

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35
Q

what are the late signs of hypoxia?

A

cyanosis, decreased BP and HR

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36
Q

what are the 4 signs of respiratory distress?

A

Tachycardia
Dyspnea
Use of accessory muscles
Hypoxia

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37
Q

what are the 4 ways that corticosteroids suppress airway inflammation?

A
  • edema of mucosa
  • in airway reactivity
  • mucus secretions
  • sensitivity to B2 adrenergic receptors
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38
Q

corticosteroids prototype: chronic

A

flunisolide (Aerobid) - inhaler


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39
Q

corticosteroids prototype: acute

A

Prednisone (methylprednisolone) - systemic

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40
Q

Always administer bronchodilators BEFORE

A

corticosteroids

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41
Q

Dysrhythmia is an

A

abnormal heart rhythm

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42
Q

What is the number 1 cause of arrhythmias?

A

hypoxia (low oxygen levels)

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43
Q

arrhythmias become significant when they

A

interfere with cardiac function and the ability to adequately perfuse the body

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44
Q

2 functions of the cardiovascular system

A
  1. Transport supplies to the cell

2. Remove waste products

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45
Q

the heart pumps ____ L per min

A

5-6 L/min

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46
Q

55% of the blood

A

is plasma

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47
Q

normal HCT levels for men and women

A

M: 42-50%
F: 40-48%

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48
Q

normal WBC (leukocytes) levels

A

5,000-10,000

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49
Q

normal HGB levels for men and women

A

M: 13-18
F: 12-16

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50
Q

normal Thrombocytes (platelets) count

A

100,000-400,000

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51
Q

4 types of blood vessels

A

Arteries, veins, capillaries, Lymphatic vessels

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52
Q

Positive inotropics ___ the force of myocardial contraction

A

increase

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53
Q

Inotropic anti-arrhythmic prototype

A

digoxin (Lanoxin)

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54
Q

Potassium (K+) normal levels

A

3.5–5.2 mEq/L

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55
Q

Calcium (Ca++) normal levels

A

8.5-10mg/dL

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56
Q

Magnesium (Mg+) normal levels

A

1.3-2.5 mEq/L

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57
Q

Effects of Digoxin

A
  • increased contractility: positive inotropic
  • increased Cardiac Output
  • decreased HR: negative Chronotropic
  • Anti-arrhythmic
  • Indirect diuretic
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58
Q

Digitalis or “loading dose” of digoxin for IV administration and oral administration

A

between 0.75- 1.5 mg with intravenous administration and 1-1.5 mg with oral administration

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59
Q

Hypokalemia

A

not enough potassium

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60
Q

SA: ___ bpm

A

60-100bpm

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61
Q

AV: ____ bpm

A

40-60bpm

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62
Q

Ventricles: ___ bpm

A

20-40bpm

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63
Q

3 main uses for digoxin

A
  1. treat heart failure
  2. treat Atrial arrhythmias
  3. treat Sinus Tachycardia
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64
Q

2 common GI-related ADEs of digoxin

A

N/V, anorexia

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65
Q

3 common CNS-related ADEs of digoxin

A

Blurred vision, diplopia, halos

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66
Q

3 common cardio-related ADEs of digoxin

A

Bradycardia, tachycardia, PVCs

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67
Q

Serious ADE of digoxin

A

ventricular fibrillation

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68
Q

6 contraindications for digoxin

A 
V tack 
V fib 
Bradycardia
Heart block ( 2nd or 3rd degree)
Bradycardia
Hypokalemia
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69
Q

What is the therapeutic level for digoxin?

A

0.5-2

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70
Q

What are the top 5 signs/symptoms of digoxin toxicity?

A 
N/V
confusion
blurred vision
Bradycardia
PVCs
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71
Q

PVC

A

premature ventricular contraction

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72
Q

What kind of patients are at risk for digoxin toxicity?

A 
Hypokalemia (not enough K)
Renal or liver failure
Large loading dose
Large maintenance doses
Infants and elderly
Hypothyroidism
Hypoxia
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73
Q

Treatment of digoxin toxicity

A 
Stop Digoxin
Tx symptomatically:
	- KCL
	- Anti-arrhythmic
	- Atropine for bradycardia
	- Digibind
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74
Q

What are the 3 main nursing interventions for digoxin?

A

K+
Explain med regime (patient teaching)
Administer w/ meals or water

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75
Q

Hold digoxin if pulse is

A

below 60 bpm

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76
Q

4 types of Arrhythmias/Dysrhythmias

A
  1. Sinus arrhythmias
  2. Atrial arrhythmias
  3. Nodal or Junctional
  4. Ventricular arrhythmias
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77
Q

Arrhythmias/Dysrhythmias are caused by changes in ___, changes in ____, or both

A

automaticity, conductivity

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78
Q

What three patient conditions can bring about Arrhythmias/Dysrhythmias?

A

Hypoxia (number 1)
Ischemia
K levels – high or low

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79
Q

What happens in stage 1 of the Na-K pump cycle?

A

Polarized or Resting or Ready State

cells around the node are in resting/polarized state – at this point sodium and calcium are normal and extracellular, potassium is intracellular

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80
Q

What happens in stage 2 of the Na-K pump cycle?

A

Depolarization or Discharge State

as electrical impulses come, the cell is depolarized
when the impulse hits, Na and Ca switch places with K as the cell contracts
so Na and Ca move intracellular, and K moves extra-cellular

P wave & QRS

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81
Q

What happens in stage 3 of the Na-K pump cycle?

A

Repolarization or Recovery State

once the electrical impulse is cast on to the next stage, the cell relaxes and repolarized - Na and K switch back to original position (so NA and Ca move back to extracellular, and K moves back to intracellular)

T wave

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82
Q

4 Classifications of Antiarrhythmic Meds

A

Class I Na Channel Blockers
Class II Beta Adrenergic Blockers
Class III Potassium Channel Blockers
Class IV Calcium Channel Blockers

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83
Q

Class I Na Channel Blockers prototype

A

lidocaine (Xylocaine)

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84
Q

Class II Beta Adrenergic Blockers prototype

A

propranolol (Inderal)

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85
Q

Class III Potassium Channel Blockers prototype

A

Amiodarone (Cordarone)

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86
Q

Class IV Calcium Channel Blockers prototype

A

verapamil (Calan)

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87
Q

How do Class I: Na Channel Blockers work?

A

Blocks the movement of Na into cardiac cells and slows conduction

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88
Q

Common ADE of Lidocaine

A

Hypotension, bradycardia, “lidocaine crazies”

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89
Q

Serious ADE of Lidocaine

A

Cardiac arrest, seizures

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90
Q

Lidocaine is used to treat

A

rapid ventricular arrhythmias

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91
Q

contraindications for lidocaine

A

Digoxin toxicity, Heart failure, heart block, Allergy to med

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92
Q

Class IA Na Channel Blocker prototype

A

Quinidine

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93
Q

Class IC Na Channel Blocker prototype

A

flecanide (Tambor)

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94
Q

How do Class II: Beta Adrenergic Blockers work?

A

Blocks the SNS, thereby slows ventricular conduction

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95
Q

Common ADE of Propranolol

A

Bradycardia, hypotension, lethargy

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96
Q

Serious ADE of Propranolol

A

bronchoconstriction

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97
Q

Propranolol is used to treat

A

rapid ventricular arrhythmias, HTN and Angina

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98
Q

Propranolol is a ___ chronotropic and a ___ inotropic

A

negative, negative

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99
Q

What is the 1st line med for antiarrhythmic for ACLS?

A

Class III: K Channel Blockers (Amiodarone)

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100
Q

Class III: K Channel Blockers (Amiodarone) are used to treat

A

life threatening arrhythmias

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101
Q

Class III: K Channel Blockers work by ____ repolarization and ____ the refractory period

A

slowing; prolonging

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102
Q

How do Class IV: Calcium Channel Blockers work?

A

Slows depolarization

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103
Q

Common ADEs of verapamil (Calcium Channel Blockers)

A

Constipation, dizziness, orthostatic hypotension, edema

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104
Q

Serious ADEs of verapamil (Calcium Channel Blockers)

A

Hypotension, bradycardia

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105
Q

Aside from treating arrhythmias, verapamil is also used to treat

A

HTN and Angina

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106
Q

5 Non-Pharmacological Treatments for Arrhythmias

A
  1. Treat underlying disorder
  2. Valsalva or carotid artery massage
  3. Defibrillate
  4. Pacemakers, AICDs
  5. Ablation
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107
Q

Rule for nursing care of arrhythmias:

A

treat the patient, NOT the monitor

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108
Q

Nursing diagnoses for arrhythmias (6)

A
  • decreased cardiac output
  • Alt in comfort
  • Alt tissue perfusion
  • Self-care deficit
  • FVE
  • Noncompliance
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109
Q

What are the 5 coronary arteries?

A
  1. aorta
  2. right coronary artery
  3. left anterior descending coronary artery
  4. circumflex coronary artery
  5. left main coronary artery
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110
Q

What are the characteristics of Stable or Classic Angina?

A
  • Relieved by rest and/or Nitroglycerine
  • Same pattern of onset, duration, and intensity
  • Predictable
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111
Q

Symptoms of angina

A

angina can spread anywhere between the belly button and the jaw, including to the shoulder, arm, elbow or hand - usually on the left side

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112
Q

3 classifications of anti-anginal medications

A
  1. Nitrates
  2. Beta Blockers
  3. Calcium Channel Blockers
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113
Q

How do all of the antianginal medications work?

A

By decreasing myocardial O2 demand and/or increasing blood supply to the myocardium

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114
Q

Organic Nitrates prototype

A

nitroglycerine (Nitrostat)

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115
Q

3 ways that nitrates work through dilation

A
  1. Dilates veins to decrease preload
  2. Dilates coronary arteries to increase myocardial flow
  3. Dilates arterioles to decrease afterload
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116
Q

All nitrates work to offset cardiac output, thereby ____ O2 demand and reducing angina

A

lowering

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117
Q

Common ADE of nitrates

A

Headache, orthostatic hypotension

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118
Q

Serious ADE of nitrates

A

Severe hypotension

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119
Q

Contraindications of nitrates

A 
Hypotension, 
Phosphodiesterase inhibitors (Viagra)
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120
Q

Hold giving nitrates if BP is

A
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121
Q

Beta-Adrenergic Blockers prototype

A

propranolol (Inderal)

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122
Q

When used PA, propranolol (Inderal) helps to give

A

long term treatment of angina

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123
Q

Common ADE for propanolol

A

Hypotension, bradycardia, lethargy

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124
Q

Serious ADE for propanolol

A

Bronchoconstriction, heart block

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125
Q

propanolol works by ____ heart rate and ___ BP, making it a ____ chronotropic and inotropic

A

decreasing, decreasing, negative

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126
Q

Calcium Channel Blockers are used to treat angina when

A

nitrates or beta blockers don’ t work

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127
Q

How do Calcium Channel Blockers work?

A

Slows the movement of extracellular Ca into the cell, which causes coronary and peripheral arterial dilation -
this decreases afterload and increases blood supply to the heart

overall, they decrease workload of the heart

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128
Q

Diuresis

A

excretion of fluid, esp water

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129
Q

Diuretics

A

medications that increase renal excretion of water and other electrolytes, and increase urine formation and urine output

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130
Q

4 categories of diuretics

A
  1. Thiazide
  2. Loop
  3. Potassium sparing or Aldosterone Antagonists
  4. Osmotic
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131
Q

Thiazides prototype

A

Hydrochlorothiazide

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132
Q

Loop prototype

A

Furosemide (Lasix)

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133
Q

K+ Sparing Aldosterone Antagonist prototype

A

Spironolactone (Aldactone)

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134
Q

Osmotic prototype

A

Mannitol (Osmitrol)

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135
Q

Thiazides are used to treat which 3 issues?

A

HTN
Edema
CHF

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136
Q

Loop is used to treat which 4 issues?

A

HTN
Edema
CHF
Renal diuresis

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137
Q

K+ Sparing Aldosterone Antagonists are used to treat which 2 issues?

A

HTN

Liver disease

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138
Q

Osmotics are used to treat which 3 issues?

A
  1. increased ICP
  2. glaucoma
  3. Oliguria/ Anuria
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139
Q

Thiazides are ___ for immediate diuresis

A

NOT

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140
Q

Loop provides ____ diuresis

A

Rapid, immediate

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141
Q

When are K+ Sparing Aldosterone Antagonists NOT to be used?

A

in renal disease

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142
Q

Osmotics are best for ____ IV use

A

Short term

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143
Q

All of the diuretics lose H20, K+, Na and Cl except ____, which results in ____ K+

A

K+ Sparing Aldosterone Antagonists; increased

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144
Q

1L of fluid = ___ kg or ____ lbs

A

1 ; 2.2

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145
Q

Normal range for Na

A

135 -145

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146
Q

Normal range for K

A

3.5 -5.2

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147
Q

Normal range for Cl

A

94-110

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148
Q

When giving diuretics, you should always monitor for

A

orthostatic hypotension

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149
Q

What time of day should you administer diuretics?

A

AM

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150
Q

Common ADE for Thiazides, Loop and Osmotics

A
  1. light headed, dizzy, orthostatic hypotension

2. hypokalemia

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151
Q

Common ADE for K Sparing

A
  1. light headed, dizzy, orthostatic hypotension

2. HYPERkalemia

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152
Q

Serious ADE for Thiazides

A

Hypokalemia

Thrombocytopenia

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153
Q

Serious ADE for Loop

A

Hypokalemia

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154
Q

Serious ADE for K Sparing

A

Hyperkalemia

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155
Q

Serious ADE for Osmotics

A

Fluid and electrolyte imbalances

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156
Q

Thrombocytopenia

A

deficiency of platelets in the blood that causes bleeding into the tissues, bruising, and slow blood clotting after injury

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157
Q

First treatment of choice for bradycardia is ____, second treatment of choice is

A

atrophy anticholinergic

second choice is anticholinergic

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158
Q

Treatment of choice for tachycardia

A

beta blocker

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159
Q

Ventricular arrhythmias originate in the ____ and are our main focus with medication because they ____

A

ventricle; are very often life-threatening

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160
Q

What is the normal procedure of the Na-K pump?

A

cells around the node are in resting/polarized state – at this point sodium is normal, extracellular, potassium is intracellular
as electrical impulses come, the cell is depolarized
when the impulse hits, Na and K switch places as the cell contracts
once the electrical impulse is cast on to the next stage, the cell relaxes and repolarized - Na and K switch back to original position

isoelectric line - time before the P wave - the cells are polarized/waiting to get impulse
impulse hits in atria, products P wave
as impulse continues down to AV node, we get small delay then the impulse continues down through the ventricles which produces the QRS
once the wave has gone through and depolarized the ventricles, once that’s finished, then the T wave comes - this marks the repolarization of the cells from the ventricles

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161
Q

isoelectric line

A

the baseline on the ECG - the flat line between the T wave and the next P wave

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162
Q

P wave represents

A

atrial depolarization

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163
Q

QRS complex

A

corresponds to the depolarization of the right and left ventricles of the human heart

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164
Q

T wave represents

A

the repolarization (or recovery) of the ventricle

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165
Q

Class I Na Channel Blockers are given given ___ for PVCs

A

intravenously

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166
Q

key safety concern for Class I Na Channel Blockers

A

you want it to say on the label, “IV use for ventricular arrhythmias” or “for cardiac use only” – DO NOT use if it says “for nerve blocks”

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167
Q

Class I Na Channel blockers are metabolized by the ____ and excreted by the ____

A

liver ; kidneys

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168
Q

Examples of sinus arrhythmias

A

bradycardia, tachycardia

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169
Q

Examples of atrial arrhythmias

A

Fibrillation or flutter: digoxin

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170
Q

Nodal/Junctional arrhythmias come from

A

the AV node

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171
Q

Examples of ventricular arrhythmias

A

PVC - premature ventricular contraction
V Tachycardia
V fibrillation

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172
Q

Bronchoconstriction is an important, serious ADE of propranolol especially if the patient has

A

underlying pulmonary disease

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173
Q

ACLS

A

advanced cardiac life support

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174
Q

Valsalva

A

exhalation against a closed – when we have a patient bear down like they’re having a bowel movement, which stimulates the vagus nerve, gets the enervation of the PSNS to help slow the heart rate

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175
Q

When performing carotid artery massage, palpate

A

only ONE side of the heart at a time

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176
Q

Ablation

A

using lasers to destroy the cells using to cause the arrhythmias

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177
Q

ALL anti-arrhythmic medications can cause

A

other arrhythmias

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178
Q

Explain procedures to patient – EVEN WHEN

A

patient is comatose - no one knows when hearing stops

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179
Q

2 main causes of angina

A 
1. increased Myocardial O2 demand
(Strenuous exercise (note that this is relative)
Stress, anxiety
Smoking 
Cold weather)
  1. decreased O2 supply to myocardium
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180
Q

Atherosclerosis

A

buildup of plaque within the vessels so that they narrow over time, as they narrow, they become less patent and its harder for blood to flow through them

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181
Q

Atherosclerosis

A

when there’s a stiffening/thickening of the vessel walls and they no longer dilate/constrict like they should

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182
Q

Atherosclerosis and Atherosclerosis have different pathology but it’s very likely that they will both

A

be occurring AT THE SAME TIME

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183
Q

diabetes melanous causes

A

vascular changes

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184
Q

If the patient is having chest pain

A

tell them to stop and rest

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185
Q

5 non-pharmalogical treatments for angina

A 
Stop smoking
Wt loss 
decreasing fat in diet
Relaxation techniques
Stress management
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186
Q

preload

A

amount of blood returning to the right side of the heart

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187
Q

When does peripheral vascular pressure fall to the lowest point?

A

diastole

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188
Q

When administering nitrates sublingually, make sure

A

they are NOT to be chewed - only put right under the tongue`

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189
Q

Patient teaching for nitroglycerin

A

take a nitroglycerin and wait 5 min, if pain is not relieved within 5 min, take a second nitroglycerin and call 911 or get to the ER

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190
Q

Patches: Transdermal Nitro can be left in place for

A

24 hours (but tolerance can develop this way)

191
Q

Preferred method for applying/removing Transdermal Nitro patches

A

use in the morning when the patient first gets up, put on the patch in the area where there’s not a lot of hair - upper arm or chest

make sure to change where you put it each time

wear it all day, then take patch off before bed – dispose of it carefully so no one can get to it, then clean the area

as a nurse, always WEAR GLOVES when handling these patches

192
Q

When giving verapamil (Calcium Channel Blockers) through IV, check BP and HR after

193
Q

When giving verapamil (Calcium Channel Blockers) PO, check BP and HR after

194
Q

Thiazide can take ___ hours to start acting

195
Q

When we talk about antibiotics that have a sulfate base (like Thiazide), know that patient may have

A

a cross-allergy

196
Q

Thiazides lowers blood pressure because

A

they’re giving off excess fluid from the vascular system

197
Q

Why are Potassium sparing or Aldosterone Antagonists not used to treat patients with renal disease?

A

because those patients can’t get rid of potassium they already have

198
Q

Oliguria

A

the production of abnormally small amounts of urine

199
Q

Anuria

A

failure of the kidneys to produce urine

200
Q

Hypertension affects ____ adults

A

75 million

201
Q

Less than ___ percent of patients diagnosed with HTN are adequately controlled

202
Q

HTN increases the risk for:

A
  • MI
  • CHF
  • CVA and hemorrhage
  • Renal disease
203
Q

Cardiac Output determines

A

systolic pressure

204
Q

PVR (peripheral vascular restriction) determines

A

diastolic pressure

205
Q

peripheral vascular restriction is determined by the

A

degree of constriction or dilation of arteries

206
Q

HR x SV =

A

cardiac output

ex. 80min x 70mL = 5600 = 5.6 L/min

207
Q

As the patient’s blood pressure starts dropping, baroreceptors

A

pick it up and are stimulated – this causes stimulation of SNS, which releases epi, and causes PV contraction

208
Q

Body’s response to hypotension: As the blood pressure is falling, there is a decrease in

A

renal blood flow (because the body is shunting blood to the heart), which stimulates the SNS

209
Q

Decrease in flow to the kidneys causes

A

Renin to be released

210
Q

First effect when Renin is released:

A

Renin will take inactive Angiotensin I and convert it to Angiotensin II, which is a very potent vasoconstrictor

211
Q

Second effect when Renin is released:

A

Renin signals Adrenals to secrete Aldosterone, which signals to the kidneys to start holding on to sodium and water

212
Q

The two effects of Renin when it’s released lead to

A

an increase in blood volume, increase in cardiac output, and increase in blood pressure

all of this increases the preload or volume

213
Q

Pre-hypertension

A

120-139/80-89

214
Q

HTN

A

140/90 or greater, usually on more than 1 occasion

215
Q

HTN Crisis:

A

210/120 or greater

216
Q

90-95% of people have ____, which no one cause that we can put our finger on (variety of issues)

A

Primary/Essential Hypertension

217
Q

Secondary Hypertension occurs in

A

5- 10% of patients

218
Q

causes of secondary hypertension

A

there’s an additional/primary diagnosis - find the cause, you can cure the hypertension

ex. may be from renal, endocrine, CNS, or renal artery problems

also can be caused from long-term steroid use, medications that cause patient to hold on to sodium and water

219
Q

long-term steroid use can cause

A

secondary hypertension

220
Q

3 ways in which HTN profoundly affects the heart

A

increased cardiac workload
arteriosclerosis
hypertrophy of myocardium

221
Q

True or false: HTN is asymptomatic

222
Q

HTN targets which 4 organs, and how?

A

heart – MI (heart attack)
brain – CVA (stroke)
kidneys – renal failure
eyes – retinopathy

223
Q

Angiotensin Converting Enzyme Inhibitors (ACE inhibitors) prototype

A

captopril (Capoten)

224
Q

How do ACE inhibitors work?

A

decrease afterload and decrease preload – so they decrease the overall workload of the heart

225
Q

ACE inhibitors are often used along with or may be combined with

A

Thiazide diuretic

226
Q

Common ADE of ACE inhibitors is a

A

dry, hacking cough (this is not responsive to any sort of cough suppressant, because it’s not coming from those receptors)

227
Q

Why do ACE inhibitors and ARBs have a black box warning for the 2nd and 3rd trimesters of pregnancy?

A

can cause severe fetal harm/fetal demise

228
Q

Patients with diabetes tend to do very well on

A

ACE inhibitors

229
Q

Serious ADE for ACE inhibitors and ARBs is

A

angioedema (swelling of the airways)

230
Q

Angiotensin II Receptor Blockers (ARBs) prototype

A

losartan (Cozaar)

231
Q

Why are calcium channel blockers good for patients w/ migraines or asthma?

A

because they can’t take beta blockers

232
Q

Common ADE for ARBs

A

URIs, dizziness, orthostatic hypotension

233
Q

remember first dose phenomenon for

A

peripherally acting alpha 1 blockers (prazosin)

234
Q

In which patients might beta blockers be the 1st line response for hypertension?

A

In patients w/ hx of MI, stable HF, angina

235
Q

With hypertensive crisis, the goal is to decrease BP ___ percent in ___ hours

236
Q

When dealing with Hypertensive Crisis, use

A

Nitropress

237
Q

Primary danger of nitropress is

A

having a stroke or MI

238
Q

Nitropress must be

A

mixed in the IV fluid

239
Q

Note: breath gets sweet almond smell when

A

cyanide levels start going up

240
Q

nursing interventions for nitropress

A

properly dilute it
IV pump
increase dose slowly
check BP every 2-3 minutes, as BP falls decrease rate
check arterial line (giving readout on monitor second-to-second)
make sure to wrap the IV bag
once BP comes down, switch the patient to a longer-acting antihypertensive

241
Q

What is the major reason why patients are admitted to the hospital and also return?

A

heart failure

242
Q

Potential nursing diagnoses for heart failure

A 
impaired gas exchange
change in levels of consciousness
decrease in urine output
peripheral edema
FVE (fluid volume excess)
activity intolerance and self-care deficits because they can’t move a lot or take care of themselves
243
Q

5 “stepped” program for HTN treatment

A
  1. Lifestyle modifications (Lose wt, exercise, stop smoking, decrease Na in diet)
  2. Diuretics (Thiazide or loop diuretics)
  3. Combination therapy (Thiazide diuretic, ACE Inhibitor or ARB, Beta Blocker, or Calcium Channel Blocker)
  4. Add a third medication
  5. Maximize drug doses
244
Q

Why is captopril great to treat DM?

A

b/c it preserves kidney function

245
Q

3 components of Black Box Warning for nitropress

A
  1. Not for IV Push
  2. Can cause excessive hypotension
  3. Can cause cyanide toxicity
246
Q

3 compensatory mechanisms involved in heart failure

A
  1. increased Sympathetic activity which increases cardiac workload
  2. Activation of the renin-angiotensin-aldosterone system: Renin converts Angiotensin I to Angiotensin II which creates high pressure or high afterload

Renin causes adrenal glands to secrete Aldosterone which encourages H2O and Na reabsorption: hi fluid or hi preload

  1. Ventricular hypertrophy- 2nd to increased afterload and increased preload
247
Q

main signs of heart failure

A
  • decreased BP, increased HR
  • decreased peripheral perfusion
  • crackles, tachypnea
  • pulmonary congestion and edema
  • FVE
  • cardiomegaly
248
Q

2-pronged goal of drug therapy for heart failure

A

Improve myocardial function

Alter compensatory mechanisms

249
Q

Nursing Diagnosis of Heart Failure Patient:

A 
Impaired gas exchange 
Altered tissue perfusion related to decrease in cardiac output (cardiac, cerebral, renal, peripheral)
decrease in C.O. r/t arrhythmias.
FVE
Activity intolerance 
Self-care deficit 
Noncompliance 
Knowledge deficit
250
Q

FVE stands for

A

fluid volume excess

251
Q

digoxin is used as drug therapy for heart failure because

A

it’s a positive inotropic and makes the heart more efficient

252
Q

Another option for heart failure is Outpatient Treatment, which involves

A

4 hours of drug treatment, usually about 2x/week

253
Q

beta blockers are used for heart failure patients who can’t take ACE inhibitors because of

254
Q

when heparin is given through IV it acts

A

immediately

255
Q

when heparin is given subcutaneously it acts

A

after 20-30 min

256
Q

Thrombus

A

blood clot

257
Q

Embolus

A

piece of blood clot breaks off and travels to the heart, brain, or lungs

258
Q

Anticoagulants are best in preventing

A

venous thrombus

259
Q

Anti platelet drugs are best in preventing

A

arterial thrombus

260
Q

Thrombolytics are best in preventing

A

lyse thrombus

261
Q

Fragmin and Lovenox are usually for

A

prevention

262
Q

Anticoagulant prototype

263
Q

What does PTT stand for and what are normal levels?

A

partial thromboplastin time

Norm: 25-35 secs

264
Q

Thrombocytopenia

A

decreased platelets - serious ADE of heparin

265
Q

Therapeutic PTT is

A

1 ½ - 2x’s norm or 38-70 secs

266
Q

Heparin antidote is

A

Protamine Sulfate

267
Q

Warfarin (Coumadin) is used for

A

Oral use/ Used in long term px or tx of clots

268
Q

What does PT stand for and what are normal and therapeutic levels?

A

PT: prothrombin time
N: 12-13 secs
therapeutic 1 ½ x’s norm or 18 secs

269
Q

Therapeutic INR is

270
Q

Antidote for Warfarin (Coumadin) is

271
Q

Anti platelets prevent ____ by interfering with ____

A

arterial thrombus; platelet adhesion

272
Q

Clopidogrel (Plavix) binds ____ to the platelet

A

irreversibly

273
Q

Thromboxane A2 Inhibitors (ASA) bind ___ to the platelet. Normal does are between ____ mg daily. ASAs are used most commonly in ____ prevention of MI and CVA.

A

irreversibly ; 81mg or 325 mg ; Long term

274
Q

Glycoprotein 11b/111a Receptor Antagonists prototype

A

Tirofiban (Aggrastat)

275
Q

PTCA

A

percutaneous transluminal coronary angioplasty

276
Q

Tirofiban is used with ____ and with ____

A

PTCA ; Heparin

277
Q

ASA, Clopidogrel (Plavix), Tirofiban (Aggrastat) are contraindicated when

A

Active bleeding
Thrombocytopenia
Tirofiban (Aggrastat) –stroke, major surgery or trauma in the last 6 weeks

278
Q

Alteplase (Activase) antidote

279
Q

Why is Alteplase (Activase) also called t-PA or tissue plasminogen activators?

A

binds to fibrin and converts tissue plasminogen to plasmin, which causes fibrinolysis (breakdown of clots)

280
Q

Alteplase (Activase) is used to treat acute thromboembolic events such as

A

MI, Pulmonary Embolism, femoral thrombus

281
Q

“Time is tissue” – door to needle time:

A

no > 30mins but no > 3 hours from onset

282
Q

Cholesterol norm

283
Q

HDL and LDL norms

A

HDL N: > 60

LDL N:

284
Q

Trigylcerides norms in M and F

A

under 200 for both

F: 35 – 135
M: 40-160

285
Q

Start drug therapy for hyperlipidemia immediately for patients with

A

signs and symptoms of CAD, DM, HTN, smokers

286
Q

drug therapy for hyperlipidemia is used to

A
  • Decrease lipids
  • prevent or delay atherosclerotic plaques
  • Promote regression of existing plaques
  • decreased morbidity and mortality from CAD
287
Q

Statins prototype

A

Lovastatin (Mevacor)

288
Q

Common ADE of Lovastatin (Mevacor)

A

v/d, constipation, abd cramps

289
Q

Serious ADE of Lovastatin (Mevacor)

A

hepatotoxicity, Rhabdomyolysis

290
Q

Rhabdomyolysis

A

A breakdown of muscle tissue that releases a damaging protein into the blood

291
Q

5 Current recommendations of AHA for all patients with CVD

A 
ACE Inhibitor
Beta Blocker
ASA daily
Statin
Nitro sl prn
292
Q

decreased O2 causes

A

impaired cellular function

293
Q

Asthma, chronic bronchitis, and emphysema are respiratory disorders characterized by what 4 things?

A
  1. Bronchoconstriction or bronchospasm
  2. Inflammation
  3. Mucosal edema
  4. Excessive mucus production
294
Q

3 therapeutic actions of Bronchodilators and Anti-Asthmatics

A

Dilate airways
Reduce inflammation
Stabilize mast cells

295
Q

B1 and B2 Adrenergic Bronchodilators Prototype

A

Epinephrine (Adrenaline)

296
Q

B2 Selective Adrenergic Bronchodilator Prototype

A

albuterol (Proventil)

297
Q

B2 Selective Adrenergic Bronchodilator is often the first choice because it’s

A

Short acting

298
Q

What is a long-term option of B2 Selective Adrenergic Bronchodilator?

A

Formoteral (Foradil)

299
Q

why must we use adrenergics cautiously with patients with DM?

A

their effects on carbohydrate metabolism and their ability to mask the common symptoms of hypoglycemia

300
Q

Anticholinergic bronchodilator prototype

A 
Atropine
ipratropium bromide (Atrovent)
301
Q

ipratropium bromide is not for acute treatment but rather

A

for daily maintenance

302
Q

Xanthine

A

a purine base found in most human body tissues and fluids

303
Q

Xanthines or “ophyllines” are stimulants that are

A

derived from xanthine and used for medical purposes

304
Q

Xanthines prototype

A

aminophylline

305
Q

Cardiac effects of xanthines

A

Increased HR, CO (+ chronotropic)

Increased Myocardial contraction (+ inotropic)

306
Q

GI effects of xanthines

A

Increased Gastric acid secretion which can lead to n/v, anorexia
Increased Risk of ulcers
Cramping and diarrhea

307
Q

Bronchus effects of xanthines

A

bronchodilator

308
Q

CNS effects of xanthines

A

Insomnia
Headache
Increased reflexes
Increased respiratory rate

309
Q

Contraindications for xanthines

A

acute gastric and peptic ulcer disease

310
Q

3 early signs of hypoxia

A

Mental confusion, restlessness, anxiety
increased Resp rate – subtle
increased HR > 100/min

311
Q

3 late signs of hypoxia

A

increased HR > 150/min
decreased BP
Cyanosis

312
Q

flunisolide (Aerobid) inhaler is for what kind of use?

A

daily use only - for chronic inflammation

313
Q

Prednisone (methylprednisolone) is best for

A

systemic, acute

314
Q

serious ADE for corticosteroids

A

Oral Candidiasis

315
Q

Common ADE for corticosteroids

316
Q

use corticosteroids cautiously in patients with what 3 issues?

A

peptic ulcer disease, HTN, DM

317
Q

Contraindications for corticosteroids

A

systemic fungal infection, TB, or any active infection

318
Q

All inhalers have

A

minimal systemic absorption

319
Q

Corticosteroids given PO have systemic ADE such as

A

HTN, peptic ulcer disease, increased blood sugar, decreased immune system

320
Q

Mast Cell Stabilizers prototype

A

cromolyn sodium (Intal)

321
Q

Mast cell stabilizers prevent the release of

322
Q

mast cell stabilizers are NOT for

A

acute treatment

323
Q

Leukotriene Inhibitors prototype

A

zarfirlukast (Accolate)

324
Q

Leukotriene Inhibitors prevent ___ but are not for ____

A

asthma attacks ; acute attack

325
Q

Serious ADE for Leukotriene Inhibitors

A

hepatic failure

326
Q

nursing diagnoses for respiratory drugs assessment

A 
Impaired gas exchange
Ineffective breathing pattern
Activity intolerance
Self-care deficit
Altered nutrition
Risk for injury
Noncompliance
Sleep pattern disturbance
Altered thought process
Knowledge deficit
Anxiety
327
Q

ischemia

A

an inadequate blood supply to an organ or part of the body, especially the heart muscles

328
Q

SA

A

sinoatrial node

329
Q

AV

A

atrioventricular node

330
Q

heart block

A

an abnormal heart rhythm where the heart beats too slowly (bradycardia) – II and III degree are most important

in this condition, the electrical signals that tell the heart to contract are partially or totally blocked between the upper chambers (atria) and the lower chambers (ventricles)

331
Q

diplopia

A

double vision

332
Q

Negative inotropics ____ force of muscular contractions, while positive inotropics ___ force of muscular contractions

A

weaken ; increase

333
Q

digibind is the antidote for

A

digoxin toxicity

334
Q

Bactericidal

A

will kill bacteria - ex. disinfectants, antiseptics, or antibiotics

335
Q

Bacteriostatic

A

a biological or chemical agent that stops bacteria from reproducing, while not necessarily killing them otherwise

336
Q

What is the goal of antibiotic therapy?

A

to cure the illness

337
Q

Infection

A

multiplication of microorganisms and pathogens throughout the body

338
Q

Colonization

A

localized microorganisms, but not necessarily and infection ex. MRSA—can be colonized but have no signs

339
Q

Inflammation

A

body’s protective response to infection

340
Q

Bacteremia

A

viable bacteria in circulation in the body (in the blood)

341
Q

Sepsis

A

infection where multiple organs are involved

342
Q

Acquired resistance

A

bacteria that was once destroyed by an antibiotic that no longer is

343
Q

Gram + (gram positive) and Gram - (gram negative)

A

if it takes up stain, it is Gram + which usually denotes the bacteria is aerobic (needs oxygen); Gram – doesn’t take up stain and is usually anaerobic

344
Q

Broad spectrum

A

antibiotic will kill a large spectrum

345
Q

Narrow spectrum

A

focuses on particular organisms—is selective

346
Q

Often will put patient on broad spectrum while waiting for

A

culture results to come back

347
Q

Nosocomial

A

infection that the patient acquired in the hospital

348
Q

Iatrogenic

A

infection that is the result of a procedure

349
Q

Hospital acquired are more difficult to treat and occur in people who

A

already have a decreased immune system

350
Q

Superinfection or Secondary Infection can occur when taking an antibiotic, as normal flora can be suppressed as well as

A

the target bacteria

351
Q

Vaginitis

A

When an antibiotic kills off some of normal flora which allows normal yeast to overgrow

352
Q

Thrush

A

white patches in mouth and oral pharynx—can make it difficult to swallow

353
Q

Treatment to recover some of the normal flora that may be killed off during antibiotic routine includes

A

yogurt with live cultures, buttermilk, probiotics (still research being done about which probiotics work best) –look for seal from pharmacy group

354
Q

What 3 types of patients are most at risk for Superinfection or Secondary Infection

A

Debilitated
Elderly
Immunosuppressed

355
Q

C+S

A

culture and sensitivity

356
Q

Culture

A

Determines the identify of the microbe

357
Q

Sensitivity

A

Determines which antimicrobial agent will be therapeutic

358
Q

Culture and Sensitivity can tell us quickly whether the bacteria is ___ or ____

A

gram -

or gram +

359
Q

MRSA

A

methicillin resistant staph aureus

360
Q

VRE

A

vancomycin resistant enteroccocus

361
Q

MDR-TB

A

multi-drug resistant TB

362
Q

PRSP

A

Penicillin resistant streptococcus pneumonia

363
Q

Recent study found that ___% of 100 million prescriptions written did not need antibiotics

364
Q

Patients in the ICU, at a large university or teaching hospital are at much higher risk for

A

Bacteria Resistance

365
Q

4 Contributing Factors to bacteria resistance

A

Widespread use of anti-microbial drugs
Interrupted treatment
Increase number of high risk patients
Location

366
Q

8 Factors that Impair Host Defense

A 
Breaks in the skin
Impaired blood supply
Malnutrition
Poor hygiene
Suppression of normal flora
Suppression of immune system
Chronic disease
Advanced age
367
Q

____ hospitalizations are because of allergic reactions

368
Q

50% of drug allergies are to what three antibiotics?

A

penicillin, ampicillins, and cephalosporins

369
Q

What are the signs of an Anaphylactic (life-threatening) allergic reaction, and how do you treat?

A

signs: Tightening of the airway, light headed, bronchoconstriction, tachycardia, hypotension, seizure

treat with subQ epinephrine and corticosteroid

370
Q

Allergic/ Hypersensitive Reaction can occur with ___ antimicrobial agents

371
Q

5 signs of localized infection

A

Redness, heat, edema, pain, drainage

372
Q

signs of systemic infection

A

Fever, increased HR and RR
Malaise, loss of E
Anorexia, n&v
May have palpable lymph nodes in the area
Labs: increased WBC, Culture and Sensitivity

373
Q

Antibiotics that inhibit cell wall synthesis interfere with

A

cell wall synthesis of bacteria—the cell then fills with water and rupture

374
Q

3 Antibiotics that inhibit cell wall synthesis

A

Penicillins
Cephalosporins
Vancomycin

375
Q

For beta-lactam ring to be effective as antibiotic, the beta-lactam ring has to remain

A

intact – if something breaks it, then they are no longer effective antibiotics

376
Q

Beta-Lactam ring Antibiotics (2 kinds)

A

Penicillins

Cephalosporins

377
Q

Allergic reactions to Penicillin happen more often than not happen on ___ exposure, not ___

A

second; first

378
Q

Patients with valvular heart disease—endocarditis are treated prophylactically with ____ before surgery

A

penicillin

379
Q

2 uses of penicillin

A

Tx gram + organisms

Bacterial endocarditis

380
Q

4 key characteristics of penicillin

A

Widely distributed
Poorly crosses the BBB
Mostly excreted unchanged by kidneys
Crosses placenta & into breast milk

381
Q

penicillinase

A

produce enzyme that destroys the beta lactum ring and make the penicillin or cephalosporin ineffective

382
Q

Augmentin is the more frequently used option today, and it’s a combination of what 2 drugs?

A

beta lactamase and penicillin

383
Q

BETA-LACTUM: Penicillin prototype

A

Penicillin G:

- bicillin, wycillin

384
Q

When Probenecid (Benemid) is taken with penicillin, it ___ the effectiveness of penicillin

385
Q

Empty stomach means

A

1 hour before eating OR 2 hours after eating

386
Q

BLACK BOX WARNING:

3 PEN Gs

A

Aqueous –only one IV!!! – must make sure it says for IV use only
Procaine
Benzathine

387
Q

Cephalosporins prototype

A

cefazolin

- IM or IV

388
Q

Cephalosporins uses (2)

A

to treat a wide variety of infections and used a lot for surgical prophylaxis to prevent post-op infection; must have completely administered 30 min to 2 hours prior to surgery start

389
Q

When Cephalosporins are given w/ Lasix or Aminoglycosides, it can cause

A

kidney damage

390
Q

If a patient takes Cephalosporins for 2 days with no relief, they should

A

come back in to the hospital/doctor

391
Q

Vancomycin act by inhibiting

A

wall synthesis

392
Q

Administer vancomycin slowly (60-90 min, even up to 2 hours) to prevent

A

red man syndrome (a release of histamine that causes this red rash, patient can become hypertensive)

393
Q

Vancomycin is used to treat severe infections, including

394
Q

Ototoxicity means a drug

A

interferes with hearing

395
Q

Nephrotoxicity

A

a drug’s creatine levels

No more than 1 gram if Creatine >2 (N=0.5-1.5)

accumulate in kidneys, leads to hematuria, drop in urine output, high levels of creatinine and BUN; can lead to full renal failure

396
Q

Serious ADE of Vancomycin

A

Ototoxicity

Nephrotoxicity

397
Q

3 types of antibiotics that inhibit protein synthesis

A

Aminoglycosides
Macrocodes
Tetracyclines

398
Q

Antibiotics that affect the ribosomes of the bacterial cells destroys the bacteria’s ability to ____, which kills the bacteria

A

synthesize protein

399
Q

Aminoglycosides prototype

A

gentamicin

400
Q

Aminoglycosides are category ___ for pregnancy

A

D – it crosses the placenta and is considered “fairly” toxic

401
Q

Aminoglycosides can be prescribed along with penicillin, but should not be

A

mixed together or given immediately one after the other—the penicillin can inactivate the aminoglycoside; the penicillin destroys the cell membrane of the bacteria which allows the aminoglycoside to get in to destroy it

402
Q

How do Aminoglycosides help treat Hepatic Coma or Hepatic encephalopathy?

A

in a normally functioning liver, the ammonia is absorbed, for patients with liver failure, the ammonia produced by bacteria in colon gets absorbed systemically and leads to encephalopathy—changes in consciousness and behavior; aminoglycosides will eliminate some of the GI bacteria that are producing the ammonia

403
Q

peak serum aminoglycoside levels:

A

30-60 min after IV dose

404
Q

trough serum aminoglycoside levels:

A

30 min before next dose

405
Q

aminoglycoside damage to vestibulocochlear nerve that can be ____. How does it start?

A

permanent; —starts with a little ringing or buzzing

406
Q

in some cases, aminoglycoside potentiates anesthetic neuromuscular blockers, which could

A

paralyze the patient or stop breathing entirely

407
Q

Serious ADE of aminoglycosides

A
  • Ototoxicity
  • Nephrotoxicity
  • Neuromuscular blockade
408
Q

When administering aminoglycosides, remember to avoid

409
Q

Macrolides prototype

A

erythromycin

410
Q

Macrolide’s can be either

A

Bacteriostatic or bacteriocidal

411
Q

erythromycin has a ___ microbial resistance

412
Q

Macrolides are used for

A

Tx resp tract infections
Skin infections
Tx gram + infections
Substitute for PCN allergies

413
Q

tetracycline can cause ____ in mother if pregnant

A

hepatic necrosis – Also has the bad effect for fetus: In fetus, gets into developing bone and teeth; long term effect of stunting growth; permanent teeth are mottled (brown) when come in—permanent

414
Q

Contraindications for tetracycline

A

Renal failure
During pregnancy (Hepatic necrosis in Mom, Effects bones and teeth in fetus)
Children up to 8 yrs
Lactating women

415
Q

When taking tetracycline, patients should be encouraged to consume ___ fluids by mouth

A

2000-3000mL

416
Q

Whether taking tetracycline or Fluoroquinolones, patients should avoid

A

Multivitamins (Iron, Ca, Mg, Al)
Dairy (Ca)
Antacids (Mg, Al)

417
Q

Antibiotics that inhibit nucleic acid synthesis

A

Fluoroquinolones

418
Q

Fluoroquinolones prototype

A

ciprofloxacin (Cipro)

419
Q

Arthropathy

A

joint disease present in children 60 years old

420
Q

The liver metabolizes ___ % of Fluoroquinolones, which is excreted in the feces, while the kidneys excrete ___ % unchanged

A

Liver met 20-40%

Kidneys excrete 15-40%

421
Q

Uses for Fluoroquinolones

A

Tx infections of Resp, GU, GI, bones, joints, skin, and soft tissue
Anthrax

422
Q

BLACK BOX WARNING for Fluoroquinolones

A

Avoid hi-impact exercise and strenuous wt lifting because it can lead to tendon rupture

423
Q

Antibiotics that inhibit metabolic pathways

A

antimetabolites – Sulfonamides

424
Q

Sulfonamides ___ the synthesis of folate in cells, which means cell can’t produce

A

inhibit;

produce nucleic acids so can’t replicate, which means death of bacteria

425
Q

Sulfonamides prototype

A

Sulfamethoxazole-trimethoprim (Bactrim, Septra)

426
Q

True or false: Sulfonamides are Bacteriostatic?

427
Q

Main use for Sulfonamides is to treat

428
Q

Contraindications for Sulfonamides

A

Late pregnancy or to newborns, b/c it can lead to kernicterus
Lactating women
babies

429
Q

phenazopyridine (Pyridium) is a ___ analgesic

A

urinary

analgesic used along with Bactrim to decrease the pain of urination for patient with UTI; pyridium can change the color of the urine to almost fluorescent orange or red

430
Q

Sulfonamides are not used for systemic infections because

A

they are excreted so quickly from the kidneys

431
Q

Kernicterus

A

the sulfonimide displaces bilirubin from its bonding sites which leads to toxic levels of bilirubin—fetus or newborn—effects developing brain

432
Q

Oral hypoglycemics can make blood sugars go

A

even lower

433
Q

serious ADE for Sulfonamides

A

rash, hives, itch, crystals in urine

434
Q

Kevin, age 2 weeks, has been hospitalized with uretovesical reflux and had been cathed 2x’s. He has developed a nosocomial infection and Septra liquid has been ordered for him. How do you intervene?

A

Do not give this! Hold and call provider.

435
Q

Stevens Johnson Syndrome is

A

A very often fatal hypersensitivity syndrome related to many kinds of antibiotics and medications (Sulfonamides, PCN, Tetracyclines, Barbiturates, Thiazides, NSAIDS), Viral Infections and Malignancies

436
Q

Signs and symptoms of Stevens Johnson Syndrome

A

Bulbous cutaneous lesions that are fluid filled

Ulceration of lips/mouth, eyelids, tongue, genitalia—generally affects mucous membranes

437
Q

Stevens Johnson Syndrome occurs mostly in

A

males from ages 10-30, most often Caucasian

438
Q

Tx for Stevens Johnson Syndrome

A 
treatment with steroids
Comfort measures—decrease pain, very painful
Dressing changes
Prevent open wounds from infection
Plenty of fluids
Stop taking the offending medication
439
Q

Clostridium Difficile is associated with the use of which antibiotics?

A

Penicillin
Cephalosporins
Fluoroquinolones

440
Q

Mild c. diff symptoms

A

Watery diarrhea 3 or >/day

Abdominal cramping & tenderness

441
Q

Severe c. diff symptoms

A

Watery diarrhea 10-15 x/day
Fever
Blood, pus in stool
Dehydration, Wt loss

442
Q

C. diff treatment methods - what is number 1?

A 
Stop current antibiotics
Vancomycin (#1)
Fidaxomicin (a Macrolide)
Fluids
Fecal transplants?
443
Q

Up until now C. diff has been almost ___ % healthcare related

444
Q

What is a drug used for heart failure as well as atrial fibrillation?

445
Q

A group of drugs used to decrease fluid retention and edema?

446
Q

What is a category of drug used to lower serum cholesterol?

447
Q

Two drug groups used for angina and hypertension?

A

Beta Blockers and Calcium channel blockers

448
Q

Remember that for angina we use what three types of drugs?

A

Nitrates, Beta Blockers, and Calcium Channel Blockers

449
Q

Hypokalemia is an adverse effect of which two categories of diuretics?

A

Loop and Thiazides

450
Q

What is one of the main ADE from anti-hypertensive drugs?

A

Hypotension

451
Q

What’s one of the prime ADE of anti-coagulants, anti-platelet or thrombolytic drugs?

452
Q

What is a drug that would decrease the absorption of oral digoxin, or almost any other drug?

453
Q

Why would we give a patient potassium chloride? And would we give it IV push?

A

To reverse the diuretic effect of hypokalemia

NO

454
Q

What is a drug I would use to reverse a digoxin-induced bradycardia?

455
Q

What type of OTC drugs might decrease the effects of antihypertensive drugs?

A

Adrenergic medications - Nasal decongestants, sinus or cold remedies

456
Q

What are 2 categories specifically that are very concerned with monitoring blood pressure?

A

Antihypertensives and nitrates/anti-anginals

457
Q

What are 2 categories of drugs where you really need to monitor the heart rate very closely?

A
  1. Digoxin (monitor PMI for full 60 sec)

2. Beta blockers

458
Q

What 2 categories of drugs are you going to be watching serum electrolyte levels?

A
  1. Diuretics

2. Digoxin

459
Q

What’s the antidote for an overdose of warfarin or coumadin?

460
Q

What’s the antidote for an overdose of heparin?

461
Q

Normal potassium level?

462
Q

What are three drug groups used to treat HTN and heart failure?

A
  1. Diuretics
  2. ACE inhibitors
  3. ARBs
463
Q

What is the best, most scientific way to choose the right antibiotic for my patient?

A

Culture and sensitivity

464
Q

3 Categories of drugs that are contraindicated in children?

A

Sulfonamides (less than 2 months)
Tetracyclines (less than 8 years old)
Fluorquinolones

465
Q

What is the drug that’s often used to treat MRSA?

A

Vancomycin

466
Q

What are the most common ADE for most oral antibiotics?

A

nausea/vomiting

467
Q

What are the two ADE from aminoglycosides?

A
  1. Ototoxicity
  2. Nephrotoxicity
    (3. Prolongs the neuromuscular blockage from medications used in anesthesia)
468
Q

What is the most serious ADE from antibiotics?

A

Diarrhea leading to C. diff and then death

469
Q

What happens when people stop taking their antibiotics too soon?

A

Develop drug resistance

470
Q

What classification of antibiotics should not be taken with dairy products?

A

Tetracyclines AND fluoroquinolones

471
Q

What category of antibiotics should not be taken that are left over and out of date?

A

Any of them! But also Tetracyclines

472
Q

What are the instructions that we give a patient on how to take their antibiotics?

A

Take the whole package. Space your doses, and take it until the medication is gone

473
Q

What’s one of the prime categories of antibiotics that we don’t want to use if the patient has renal failure?

A

Aminoglycosides

Pharmacology (6 decks)

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